高血压病常合并全身细小动脉(肾、心、胰、脑)硬化性病变。细小动脉硬化症的中度高血压长期持续,就会引起细小动脉的透明样变性,使血管壁肥厚和管腔狭窄。重症高血压时,内皮细胞由于反应性增殖而形成多层化和纤维蛋白样坏死。透明样变性的机制与血浆成分和结缔组织增加有关。所有高血压性血管病变均可见间质结缔组织,特别是胶原蛋白沉着过剩,血管硬度增加,弹性减少和血管壁肥厚等。事实上,动物实验证明,心血管系统有明显的胶原蛋白合成亢进。目前,测定血管壁胶原蛋白是客观评价血管病变,特别是动脉硬化症的生化指标。现将作者有关心血管胶原代谢的生化动物试验研究结果介绍如下: 一、胶原代谢的生化指标 Hypertension often complicated by small arteries (kidney, heart, pancreas, brain) sclerosis. Small arteriosclerosis in the long-term sustained high blood pressure, it will cause the transparent degeneration of small arteries, so that the vascular wall hypertrophy and stenosis. In severe hypertension, endothelial cells develop multilayered and fibrinoid necrosis due to reactive proliferation. Transparent degeneration of the mechanism and the plasma composition and connective tissue increased. All hypertensive vascular lesions are visible interstitial connective tissue, especially collagen hyperparathyroidism, increased vascular stiffness, reduced elasticity and vascular wall hypertrophy. In fact, animal experiments show that the cardiovascular system has obvious collagen synthesis hyperthyroidism. Currently, the determination of vascular wall collagen is an objective assessment of vascular disease, especially atherosclerosis biochemical indicators. Now the author of cardiovascular biochemical metabolism of animal experimental results are described below: First, the biochemical indicators of collagen metabolism